Thromboxane prostanoid signaling in macrophages attenuates lymphedema and facilitates lymphangiogenesis in mice : TP signaling and lymphangiogenesis.
Lymphangiogenesis
Lymphedema
Macrophage
Thromboxane
Journal
Molecular biology reports
ISSN: 1573-4978
Titre abrégé: Mol Biol Rep
Pays: Netherlands
ID NLM: 0403234
Informations de publication
Date de publication:
Oct 2023
Oct 2023
Historique:
received:
26
04
2023
accepted:
21
06
2023
medline:
26
9
2023
pubmed:
4
8
2023
entrez:
4
8
2023
Statut:
ppublish
Résumé
Accumulating evidence suggests that prostaglandin E Lymphedema was induced by the ablation of lymphatic vessels in mouse tails. Compared with wild-type mice, tail lymphedema in Tp-deficient mice was enhanced, which was associated with suppressed lymphangiogenesis as indicated by decreased lymphatic vessel area and pro-lymphangiogenesis-stimulating factors. Numerous macrophages were found in the tail tissues of Tp-deficient mice. Furthermore, the deletion of TP in macrophages increased tail edema and decreased lymphangiogenesis and pro-lymphangiogenic cytokines, which was accompanied by increased numbers of macrophages and gene expression related to a pro-inflammatory macrophage phenotype in tail tissues. In vivo microscopic studies revealed fluorescent dye leakage in the lymphatic vessels in the wounded tissues. The results suggest that TP signaling in macrophages promotes lymphangiogenesis and prevents tail lymphedema. TP signaling may be a therapeutic target for improving lymphedema-related symptoms by enhancing lymphangiogenesis.
Sections du résumé
BACKGROUND
BACKGROUND
Accumulating evidence suggests that prostaglandin E
METHODS AND RESULTS
RESULTS
Lymphedema was induced by the ablation of lymphatic vessels in mouse tails. Compared with wild-type mice, tail lymphedema in Tp-deficient mice was enhanced, which was associated with suppressed lymphangiogenesis as indicated by decreased lymphatic vessel area and pro-lymphangiogenesis-stimulating factors. Numerous macrophages were found in the tail tissues of Tp-deficient mice. Furthermore, the deletion of TP in macrophages increased tail edema and decreased lymphangiogenesis and pro-lymphangiogenic cytokines, which was accompanied by increased numbers of macrophages and gene expression related to a pro-inflammatory macrophage phenotype in tail tissues. In vivo microscopic studies revealed fluorescent dye leakage in the lymphatic vessels in the wounded tissues.
CONCLUSIONS
CONCLUSIONS
The results suggest that TP signaling in macrophages promotes lymphangiogenesis and prevents tail lymphedema. TP signaling may be a therapeutic target for improving lymphedema-related symptoms by enhancing lymphangiogenesis.
Identifiants
pubmed: 37540456
doi: 10.1007/s11033-023-08620-0
pii: 10.1007/s11033-023-08620-0
pmc: PMC10520203
doi:
Substances chimiques
Prostaglandins
0
Thromboxanes
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
7981-7993Subventions
Organisme : Ministry of Education, Culture, Sports, Science and Technology
ID : 21K09776
Organisme : Ministry of Education, Culture, Sports, Science and Technology
ID : 22K08856
Informations de copyright
© 2023. The Author(s).
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